Glucosamine, a sugar-like compound your body uses to build cartilage, is among the most popular dietary supplements sold in the United States. According to Health WorldNet, Americans spent $872 billion on glucosamine in 2008. Studies evaluating glucosamine’s usefulness for treating osteoarthritis have produced inconsistent results, but many people believe their symptoms improve while taking glucosamine-containing supplements. Concerns that glucosamine could interfere with insulin activity or glucose metabolism have been laid to rest.
Hexosamines
A hexose is a six-carbon sugar molecule, such as glucose or galactose. In your body, hexoses serve as fuel sources and as precursors for other important molecules, such as glucosamine and galactosamine, which are called hexosamines. Hexosamines are simply hexose sugars to which a nitrogen-containing amino group has been attached. Scientists believe that large amounts of hexosamines in your cells contribute to the production of substances that disrupt glucose metabolism and interfere with insulin activity.
Diverse Uses
Glucosamine is found in almost all of your tissues, but it is concentrated in your joints, where it serves as a precursor for glycosaminoglycans, or GAGs, which are important constituents of cartilage and joint fluid. Two principal glucosamine-derived GAGs, hyaluronic acid and keratan sulfate, tend to disappear from your joints as you age. Supplemental glucosamine is readily absorbed from your intestine and incorporated into your cartilage, but it is also used elsewhere in your body to add glucose molecules to proteins and lipids. When present in high concentrations, some of these “glycosylated” proteins and lipids appear to contribute to insulin resistance and diabetes.
Animal Studies
A 2008 review in “Endocrinology and Metabolism” cited the importance of hexosamines in setting the stage for insulin resistance, stating that increased hexosamine levels might even be necessary for the development of diabetes. Early laboratory studies evaluating the effects of glucosamine supplementation showed that it did, in fact, increase insulin resistance in rodents, raising concerns that glucosamine could precipitate or worsen diabetes in humans. However, these studies routinely employed intravenous infusions of glucosamine that delivered much higher doses than you could obtain by taking supplements at any recommended dosage.
No Effect on Insulin
In 2010, following an extensive review of research done to date, experts from the United States, Canada, Denmark and the United Kingdom concluded that glucosamine does not affect your fasting blood glucose level, your response to insulin or your body’s ability to metabolize glucose when it is taken at “any oral dose level in healthy subjects, individuals with diabetes or those with impaired glucose tolerance.” In other words, glucosamine appears to be safe even for diabetics, because it does not appear to block the effects of insulin or raise your blood glucose level.
Considerations
Glucosamine does not interfere with insulin’s activity when it is taken at recommended doses: 500 mg three times daily is the usual dose. However, large, long-term studies of glucosamine’s effects on diabetics and other insulin-resistant populations have not been conducted. Therefore, you must weigh the risks and benefits of taking glucosamine before adding it to your daily regimen. Glucosamine does not improve arthritis symptoms for everyone, so ask your doctor if glucosamine is appropriate for you. If you have diabetes and decide to take glucosamine, monitor your blood glucose level frequently.
References
- “American Family Physician”; Glucosamine; S. Dahmer, et al.; August 2008
- Health WorldNet: Glucosamine – The Bubble Is Burst…Maybe
- “Endocrinology and Metabolism”; Cross-Talk between GlcNAcylation and Phosphorylation: Roles in Insulin Resistance and Glucose Toxicity; R.J. Copeland, et al.; July 2008
- “Diabetes/Metabolism Research and Reviews”; A Comprehensive Review of Glucosamine Use and Effects on Glucose Metabolism in Normal and Diabetic Individuals; R.R. Simon, et al.; January 2011



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